Acrylamide is a neurotoxic agent which produces a central-peripheral distal axonopathy. Industrial workers exposed to acrylamide display ataxia, loss of deep tendon reflexes, loss of position and vibrational senses, paresthesis, and numbness. While a good deal of information has accumulated on the histopathology and biochemistry of the neuropathy, little is known about the pathophysiology of the neuropathy. Moreover, what is known generally pertains to functional defects in proprioception and are primarily concerned with the peripheral nervous system. In the proposed research, the influence of acrylamide on non-proprioceptive receptors and their terminals in the spinal cord will be studied. The discharge patterns from type I and type II slowly adapting receptors and pacinian corpuscles in the hairy skin of cats will be observed in normal and acrylamide-intoxicated cats. Some of the important observations will be the characteristic discharge from the receptors, the number of receptors which are active and the conduction velocity of their afferent fibers. Primary afferent terminal function will be accessed using several measures of terminal viability. First, dorsal root potentials (DRP) will be recorded and the size and shape of the DRP noted. Second, space constants will be estimated from the DRP to detect any degeneration of the afferent terminal. Third, throughput resulting from the incoming afferent volley to the primary afferent terminal will be determined by estimating the critical input. Lastly, excitability of the primary afferent terminals will be assessed by intraspinal current injection. Morphological studies will aid in the verification of degeneration. These studies will be performed in normal and acrylamide-poisoned cats. The changes observed in receptor and primary afferent terminal function will be correlated with the pathology and neurological deficits associated with acrylamide neuropathy. Also, since the pathology and neurological deficits associated with this neuropathy are similar to other chemically-induced neuropathies (making acrylamide an excellent model for these studies) the results will be frther correlated to those in other axonopathies.